Abstract
The hypoxic mechanisms responsible for the appearance of NRBC in fetal circulation are still unknown. We set forth to determine the impact of placental insufficiency induced by two distinct pathways [chronic hypoxia or chronic nitric oxide (NO) inhibition with NG-nitro-L-arginine methyl ester (L-NAME)] or both, on fetal NRBCs and erythropoietin (EPO) levels in an animal model of IUGR.
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